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T J Ruigrok

Publications and source records attributed to T J Ruigrok.

108 records · Page 6Linked to original sources
PubMed1981

The effect of dimethylsulfoxide on the calcium paradox.

Reperfusion of isolated rat hearts with calcium-containing solution after a short period of calcium-free perfusion results in irreversible cell damage (calcium paradox). Experiments were undertaken to study the effect of dimethylsulfoxide (DMSO) on the occurrence of the calcium paradox in rat heart muscle. DMSO (1.4 mol/l) was added to the calcium-free or the reperfusion medium. Cell damage was quantitated in terms of creatine kinase (CK) release, cardiac electrogram (CEG) changes, and ultrastructural damage. Reperfusion with calcium-containing solution without DMSO after calcium-free perfusion with DMSO resulted in massive release of CK, electrical arrest of the ventricles, and formation of contraction bands. Nearly 100% of the cells displayed the calcium paradox damage. Reperfusion with calcium-containing solution with DMSO after calcium-free perfusion without DMSO resulted in a moderate release of CK, and electrical arrest of the ventricles. The myofibrils remained in a relaxed state. Only 4% of the cells displayed the calcium paradox damage. These results indicate that DMSO does not protect rat hearts against the effects of calcium-free perfusion that predispose the myocardium to the calcium paradox. The calcium paradox damage is reduced, however, when DMSO is present during the reperfusion phase.

Animals↗
PubMed1980

The effect of hypothermia on the occurrence of the calcium paradox.

Reperfusion of isolated rat hearts with Ca2+-containing medium, after a short Ca2+-free perfusion period, results in irreversible cell damage (calcium paradox). In this investigation the effect of hypothermia during (a) the Ca2+-free perfusion period and (b) the phase of reperfusion with Ca2+-containing medium was studied. Failure of the heart to recover mechanical activity, and creatine kinase release were used to define cell damage. Ca2+-free perfusion was performed at 37 degrees, 30 degrees, 25 degrees and 20 degrees C. Hypothermia during the Ca2+-free period was unable to prevent the calcium paradox. At 37 degrees C a Ca2+-free perfusion was perfusion period of 4 min was sufficient to lead to failure of the hearts to recover mechanical activity and to induce massive enzyme release upon reintroduction of Ca2+. At 20 degrees C the Ca2-free perfusion had to be continued for 25 min to induce failure to recover mechanical activity, and for 80 min to induce massive enzyme release upon reperfusion with Ca2+-containing medium. Hypothermia (10 degrees - 15 degrees C) during the reperfusion phase resulted in a moderate release of creatine kinase. Massive enzyme release occurred as soon as the temperature of the perfusate was raised above 25 degrees C.

Animals↗
PubMed1980

The effect of verapamil on the calcium paradox.

Reperfusion of isolated rat hearts with calcium-containing medium after a short period of calcium-free perfusion results in irreversible cell damage (calcium paradox). Experiments were undertaken to determine whether the slow-channel calcium-antagonist drug verapamil protects calcium-deprived rat heart muscle against the consequences of readmitting calcium. Cell damage was quantitated in terms of creatine kinase (CK) release, depletion of endogenous creatine phosphate (CP) and adenosine triphosphate (ATP) stores, development of contracture as measured by longitudinal shortening of the left ventricle, and ultrastructural damage. Verapamil (1 mg/l) did not reduce the initial rate of CK release during reperfusion with calcium but reduced the initial rate at which myocardial CP and ATP stores were depleted and decreased the shortening of the longitudinal axis of the left ventricle. After 30 seconds of reperfusion the mean sarcomere length was significantly greater in the verapamil-treated hearts. These results can be interpreted to mean that inhibition of calcium inflex via the slow channels does not protect heart muscle against the deleterious effects of readmitting calcium after a period of calcium-free perfusion.

Adenosine Triphosphate↗
PubMed1978

The calcium paradox: metabolic, electrophysiological, contractile and ultrastructural characteristics in four species.

The effect of transient depletion and repletion of calcium upon the electrophysiological activity, contractile activity, coronary flow, tissue energy metabolism and the cellular leakage of metabolites and creatine kinase has been characterized in the rat heart and now has been compared with the mouse, guinea pig and rabbit heart. The sudden and massive damage (the calcium paradox) which occurred in the rat was observed in all species studied. While fine differences between species were detectable, the basic principles and damaging effects of sudden transmembrane calcium fluxes would appear to be common to all species.

Animals↗
PubMed1976

Acid-base curve nomogram for dog blood.

Pooled canine blood of different hemoglobin concentration was equilibrated with two carbon dioxide tensions and the resulting pH's of the samples were measured at 38 degrees C. Readings obtained provided data for the construction of a cartesian nomogram for the dog, based on the pH/log pCO2 coordinate system. The nomogram can be used to evaluate both respiratory and non-respiratory acid-base parameters. For contrast, a control nomogram on human blood was also constructed. Both nomograms show broad similarity. This is to be expected as the normal criteria used to define base excess relating to dog blood are the same as those used for human blood. Nonetheless, base excess and buffer base calculations using the nomogram for the dog and that for man show a deviation of 2.5-10%, and we consider this deviation to be more due to a species difference than to any summated experimental error.

Acid-Base Equilibrium↗
PubMed1975

The calcium paradox: a reaffirmation.

Perfusion of isolated rat hearts with a Ca-2+-containing medium, after a Ca2+-free perfusion period, results in an irreversible loss of electrical and mechanical activity of the heart, as well as a large release of intracellular components such as lactate dehydrogenase. These phenomena can be evoked, when hearts are perfused at a constant perfusion pressure or at a constant flow rate. Evidence is provided that recovery of the mechanical activity of the heart is not a requisite for lactate dehydrogenase release.

Animals↗
PubMed1969

Relation of mitochondrial phospholipase A activity to mitochondrial swelling.

Assays of mitochondrial phospholipase A activity and mitochondrial swelling demonstrated that the phospholipase A activity is related to the swelling under the experimental conditions used. Both were stimulated by added free fatty acid and CaCl(2), not affected greatly by the addition of monoacyl phosphoglycerides, and inhibited by EDTA. The amount of fatty acid hydrolyzed from endogenous phosphatidyl ethanolamine and phosphatidyl choline during swelling was calculated to be 20-30 times less than the amount of added free fatty acid that gave comparable swelling. Under the experimental conditions about 4% of the phospholipid was hydrolyzed. Mitochondrial swelling was studied by electron microscopy and turbidity measurements. The results found were in agreement, whether oleic acid was present or not, except for those values obtained after very brief incubation (1 min) and after incubation for longer than 35 min. The lack of direct proportion between swelling and the concentration of lysosomes present indicated that the swelling is related mainly to mitochondrial phospholipase A, although swelling due to contaminating lysosomes cannot be excluded entirely. The temperature dependence of spontaneous, fatty acid-induced, or CaCl(2)-induced swelling suggested that enzymatic activities are responsible for swelling.

Animals↗
PubMedDate not supplied

Heterotopic heart transplantation alters high-energy phosphate metabolism irrespective of cardiac allograft rejection.

This study was undertaken to validate the potential of 31P magnetic resonance spectroscopy (MRS) as a noninvasive alternative for transvenous endomyocardial biopsy in detecting cardiac allograft rejection. Donor hearts from either Lewis rats (L) or Brown-Norway rats (BN) were transplanted into the neck of L rats resulting in a non-rejecting group L-L and a rejecting group L-BN. L-L and L-BN rats were serially studied by means of 31P MRS from postoperatine day 1-8. In addition, rejection was confirmed by histology. A similar, marked decrease in phosphocreative/beta- adenosinetriphosphate (PCr/ATP) ratio from day 1-3 was observed in both L-L and L-BN hearts. This ratio levelled off on postoperative day 3 and remained depressed on subsequent postoperative days in both groups, although histology showed an increase in the severity of rejection in L-BN. However, the PCr signal/noise ratio in L-BN started to decrease after day 4, coinciding with the histologic evidence of severe rejection (score IV), whereas in L-L hearts (score 0) this ratio remained unaltered until day 8. Since high-energy phosphate metabolism is affected by the unloaded status of the heterotopically transplanted heart, irrespective of rejection, the PCr/ATP ratio appears not to be a specific marker for the detection of acute rejection in this model. In contrast, the PCr S/N ratio appears to be a specific and sensitive marker of acute rejection, but only in a late, severe stage.

Animals↗
PubMedDate not supplied

The effect of hypothermia during the period of calcium repletion on the calcium paradox.

Reperfusion of an isolated heart with a calcium-containing solution after a short calcium-free perfusion may result in irreversible cell damage: the calcium paradox. In this investigation the effect of hypothermia during reperfusion with calcium-containing solution on the calcium paradox damage in the isolated rat heart was studied. In addition, the effect of pre-cooling the heart during the calcium-free period was investigated. Creatine kinase release was used to define cell damage. Normothermic (37 degrees C) calcium-free perfusion followed by normothermic reperfusion with calcium-containing solution resulted in a massive release of CK. When the normothermic calcium-free perfusion was followed by hypothermic (10 degrees C) calcium-containing reperfusion, CK release was reduced by 20% (P less than 0.005). This CK release during reperfusion was further reduced by 55% and 80% when the normothermic calcium-free perfusion was followed by 5 or 10 min respectively of hypothermic calcium-free perfusion prior to the hypothermic calcium-containing reperfusion. The results show that hypothermia during the period of calcium repletion retards the sequence of events which ultimately results in release of large amounts of intracellular components.

Animals↗
PubMedDate not supplied

No evidence of oxygen free radicals-mediated damage during the calcium paradox.

Reperfusion of an isolated mammalian heart with a calcium-containing solution after a brief calcium-free perfusion results in irreversible cell damage: the calcium paradox. We investigated whether the calcium paradox is associated with oxidative damage. We measured the tissue changes of glutathione status and the release of oxidized glutathione from isolated perfused rabbit hearts as indicators of cellular oxidative events. After 10 min of calcium-free perfusion, tissue content of reduced (GSH) and oxidized (GSSG) glutathione, and of protein and non-protein sulfhydryl groups were not significantly different from control values. Restoration of the calcium concentration resulted in an immediate and massive release of GSH and a depletion of tissue content of GSH, GSSG, and non-protein sulfhydryl groups. However, only a minimal release of GSSG into the coronary effluent was observed. In addition, the characteristic features of the calcium paradox were present: development of an irreversible contracture and massive release of creatine kinase. The calcium paradox did not lead to a decrease of the tissue content of protein sulfhydryl groups. These observations indicate that the calcium paradox is not associated with oxidative damage.

Animals↗
PubMedDate not supplied

A retrograde double-labeling technique for light microscopy. A combination of axonal transport of cholera toxin B-subunit and a gold-lectin conjugate.

A light microscopical, non-fluorescent, retrograde double-labeling technique is described. Cholera toxin B-subunit (CTb) and a conjugate of wheatgerm agglutinin and bovine serum albumin coupled to 10 nm gold particles (gold-lectin) are both excellent retrograde tracers and, when visualized by means of immunohistochemistry and silver intensification, respectively, may be readily identified within the same cell. This light microscopical retrograde double-labeling technique is illustrated in rat with experiments designed to investigate the collateralisation (1) of vestibular neurons to the spinal cord and oculomotor complex, (2) of spinal neurons to the left and right lateral reticular nucleus, and (3) of inferior olivary neurons to the uvula of the cerebellum. Advantages over fluorescent double-labeling experiments are found in the fact that the diaminobenzidine reaction product as well as the silver/gold deposits do not fade and can be examined in counterstained sections. Moreover, the injection sites can be kept quite small and may be guided by electrophysiological recording through the injection pipette.

Animals↗
PubMedDate not supplied

Calcium paradox: changes in high-energy phosphate compounds of isolated perfused rat hearts.

When isolated rat hearts are perfused with Ca2+-containing medium, after a brief Ca2+-free period, irreversible cell damage occurs (calcium paradox). This phenomenon is concomitant with a rapid consumption of myocardial high-energy phosphate stores, prior to the appearance of these compounds in the effluent perfusion medium. A possible mechanism for the origin of myocardial necrosis, caused by intracellular Ca2+ overload, is discussed.

Adenine Nucleotides↗
PubMedDate not supplied

Influence of ATP or oxygen plus substrate on occurrence of the calcium paradox.

Reperfusion of Ca2+-deprived rat hearts with Ca2+-containing medium results in irreversible cell damage (calcium paradox). In this study this type of cell damage was studied in the anoxic rat heart, in the presence and absence of glucose. Creatine kinase (CK) release was used to define cell damage. Hearts were perfused successively with Ca2+-containing medium (30 min), Ca2+-free medium (5 min), and Ca2+-containing medium (5 min). In the presence of glucose, myocardial ATP was maintained at a fairly high concentration. Reperfusion with Ca2+ resulted in an immediate and massive release of CK. In the absence of glucose, the ATP concentration was almost zero after 30 min. Reperfusion with Ca2+ did not result in release of CK. Massive release occurred as soon as these hearts were reoxygenated. It is concluded that this type of calcium-induced cell damage only occurs in the presence of ATP, or oxygen plus substrate. Mitochondria most likely play a major role in the occurrence of the calcium paradox because of their ability to accumulate huge amounts of Ca2+ under these conditions.

Adenosine Triphosphate↗
PubMedDate not supplied

A phosphorus-31 nuclear magnetic resonance study of myocardial ATP content during postischemic low calcium reperfusion.

Postischemic reperfusion injury can be modified by transient low calcium (Ca2+) reperfusion, although the data on the optimal [Ca2+] are controversial. High-energy phosphates and contractile function of isolated perfused rat hearts (37 degrees C, 300 beats/min) were studied simultaneously during global ischemia (30 min) and reperfusion (10 min at [Ca2+] = 1.3, 0.05, 0.1, 0.3, 0.5 and 0.7 mmol/l, followed by 20 min at [Ca2+] = 1.3 mmol/l), using phosphorus-31 nuclear magnetic resonance (31P NMR) spectroscopy. Reperfusion with 1.3 mmol/l Ca2+ after 0.05 or 0.1 mmol/l Ca2+ largely abolished the recovery of ATP obtained during initial low Ca2+ reperfusion (calcium paradox effect). A [Ca2+] of 0.3 mmol/l was sufficiently high to prevent this detrimental effect; at the same time this concentration was sufficiently low to cause a substantial recovery of ATP, which was maintained upon switching to 1.3 mmol/l Ca2+. Recovery of ATP did not correlate with recovery of contractile function.

Adenosine Triphosphate↗
PubMedDate not supplied

Autogenous vein graft thrombosis following exposure to calcium-free solutions (calcium paradox).

The morphological and functional effects of calcium-free and calcium-containing solutions on canine jugular vein intima were examined under conditions which closely resemble those techniques currently employed in peripheral vascular and aortocoronary bypass surgery. Veins that had been exposed only to calcium-containing solutions remained patent for the duration of the experimental period. Vein perfusion with a calcium-free solution, however, resulted in disruption of the jugular vein intima once calcium ions were reintroduced. Autogenous as a femoral arterial graft became thrombosed within 60 minutes. It is therefore suggested that vein grafts of autogenous origin be irrigated with calcium-containing solutions to prevent intimal damage and thrombosis.

Animals↗